Obesity is a common condition and a major public health problem in developed nations including the United States of America. Today, 64.5% of American adults, about 127 million people, are either overweight or obese. Data suggest that 300,000 Americans die prematurely from obesity-related complications each year. Many children are overweight or obese in the United States; hence, the steady increase in the number of overweight Americans is expected to continue. It has been estimated that obesity costs the United States approximately $100 billion annually in direct and indirect health care expenses and in lost productivity. This trend is also apparent in many other developed countries.
Morbid obesity is defined as possessing either a body weight more than 100 pounds greater than normal or a body mass index (BMI) greater than 40 kg/m2. Approximately 5% of the U.S. population meets at least one of these definitions. A BMI greater than 30 kg/m2 is associated with significant co-morbidities. Morbid obesity is associated with many diseases and disorders including, for example, diabetes, hypertension, heart attacks, strokes, dyslipidemia, sleep apnea, Pickwickian Syndrome, asthma, lower back and disc disease, weight-bearing osteo-arthritis of the hips, knees, ankles and feet, thrombophlebitis and pulmonary emboli, intertriginous dermatitis, urinary stress incontinence, gastroesophageal reflux disease (GERD), gallstones, and sclerosis and carcinoma of the liver. In women, infertility, cancer of the uterus, and cancer of the breast are also associated with morbid obesity. Taken together, the diseases associated with morbid obesity markedly reduce the odds of attaining an average lifespan and raise annual mortality in affected people by a factor of 10 or more.
Current treatments for obesity include diet, exercise, behavioral treatments, medications, surgery (open and laproscopic) and endoscopic devices. Also, additional treatments for obesity are currently being evaluated in clinical trials. However, a high efficacy pharmaceutical treatment has not yet been developed. Further, short-term and long-term side effects of pharmaceutical treatments may concern consumers, pharmaceutical providers, and/or their insurers. Generally, diet or drug therapy programs have been disappointing and fail to bring about significant, sustained weight loss in the majority of morbidly obese people.
Currently, most morbid obesity operations are, or include, gastric restrictive procedures, involving the creation of a small (e.g., 15-35 mL) upper gastric pouch that drains through a small outlet (e.g., 0.75-1.2 cm), setting in motion the body's satiety mechanism. About 15% of morbid obesity operations done in the United States involve gastric restrictive surgery combined with a malabsorptive procedure. Typical malabsorptive procedures divide small intestinal flow into a biliary-pancreatic conduit and a food conduit. Potential long-term problems with surgical procedures, including those seen after any abdominal procedure, are notorious and can include, for example, ventral hernia and small bowel obstruction. In addition, long-term problems specific to bariatric procedures can include, for example, gastric outlet obstruction, marginal ulceration, protein malnutrition, and vitamin deficiency.
Other surgical strategies for treating obesity include endoscopic procedures, many of which are still in development. Endoscopically placed gastric balloons restrict gastric volume and result in satiety with smaller meals. Endoscopic procedures and devices to produce gastric pouch and gastrojejunal anastomosis to replicate laparoscopic procedures are also in development. These procedures, however, are not without risks.
Gastric electric stimulation (GES) and vagal stimulation (BBLOC) are other procedures currently in clinical trials. Both GES and VBLOC employ an implantable, pacemaker-like device to deliver low-level electrical stimulation to the stomach (GES) or vagus nerve (VBLOC). The procedures involve a surgeon suturing electrical leads to the outer lining of the stomach wall in GES vagus nerve in VBLOC. The leads are then connected to a device that may be implanted in the patient, for example, just under the skin in the abdomen. An external programmer may communicate a prescribed level of electrical stimulation appropriate for the patient. The TRANSCEND (Medtronic Transneuronix Inc., Mount Arlington, N.J.) implantable gastric stimulation device for GES is currently being evaluated for the treatment of obesity. The MAESTRO RF2 System (EnteroMedics, Inc., St. Paul, Minn.), an implantable vagal stimulation device for VBLOC, is currently in U.S. trials for the treatment of obesity. Exemplary treatments and treatment systems can be found in U.S. patent application Ser. No. 12/359,317, filed on Jan. 25, 2009, Ser. No. 11/539,645, filed on Oct. 9, 2006, and Ser. No. 12/030,222, filed on Feb. 13, 2008, PCT Patent Application No. PCT/US08/56479, and U.S. Pat. No. 6,901,295, which are incorporated herein by reference.
U.S. Pat. No. 6,993,391 discloses an apparatus that “comprises a control unit 190, and one or more electrodes 200 applied to or in a vicinity of respective sites of the arterial supply 130 of the patient's small intestine 120. If appropriate, some or all of electrodes 200 may be placed on the superior mesenteric artery 110, or in a vicinity thereof. Typically, control unit 190 drives electrodes 200 to apply signals which cause a controllable level of constriction of the arteries to which these electrodes are coupled. Alternatively or additionally, other transducers (not shown) are implanted in the patient in a vicinity of arterial supply 130, and are driven by control unit 190 to induce some or all of the arteries in supply 130 to contract. As appropriate, these transducers may induce this contraction using mechanical or chemical means. The constriction produced by apparatus 118 preferably transiently and controllably reduces the blood flow to small intestine 120, and thereby reduces the total number of calories which are ultimately absorbed into the patient's bloodstream during and after eating a meal.” However, this treatment method only targets the superior mesenteric artery (SMA) which is the arterial supply of small intestine in order to cause malabsorption, which has limited efficacy and does not curtail appetite or induce satiety and hence does not decrease caloric intake. In addition, efficacy of stimulating only SMA may decrease over time due to development of collateral blood supply from other arteries of gastrointestinal vasculature.